Astaxanthin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy via the ROS/MAPK Pathway in Mice

Marine Drugs

Jingjing Li²  Fan Wang²  Yujing Xia²  Weiqi Dai²  Kan Chen²  Sainan Li²  Tong Liu²  Yuanyuan Zheng²  Jianrong Wang³  Wenxia Lu³  Yuqing Zhou¹  Qin Yin¹  Jie Lu²  Yingqun Zhou²  Chuanyong Guo² 

[1] The First Affiliated Hospital of Soochow University, Suzhou 215006, China; E-Mails:;Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China; E-Mails:;The First Clinical Medical College of Nanjing Medical University, Nanjing 210029, China; E-Mails:

关键词: hepatic ischemia reperfusion;    oxidative stress;    astaxanthin;    reactive oxygen species;   

DOI  :  10.3390/md13063368

来源: mdpi

【 摘 要 】

Background: Hepatic ischemia reperfusion (IR) is an important issue in complex liver resection and liver transplantation. The aim of the present study was to determine the protective effect of astaxanthin (ASX), an antioxidant, on hepatic IR injury via the reactive oxygen species/mitogen-activated protein kinase (ROS/MAPK) pathway. Methods: Mice were randomized into a sham, IR, ASX or IR + ASX group. The mice received ASX at different doses (30 mg/kg or 60 mg/kg) for 14 days. Serum and tissue samples at 2 h, 8 h and 24 h after abdominal surgery were collected to assess alanine aminotransferase (ALT), aspartate aminotransferase (AST), inflammation factors, ROS, and key proteins in the MAPK family. Results: ASX reduced the release of ROS and cytokines leading to inhibition of apoptosis and autophagy via down-regulation of the activated phosphorylation of related proteins in the MAPK family, such as P38 MAPK, JNK and ERK in this model of hepatic IR injury. Conclusion: Apoptosis and autophagy caused by hepatic IR injury were inhibited by ASX following a reduction in the release of ROS and inflammatory cytokines, and the relationship between the two may be associated with the inactivation of the MAPK family.

【 授权许可】

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© 2015 by the authors; licensee MDPI, Basel, Switzerland.